Coronary obstructive disease in man occurs in the large branches of the coronary arteries, and causes the controlling resistance to flow to be transferred from the arterioles to the proximal artery at the site of the partially obstructing atherosclerotic plaque. Patients with coronary obstruction ranging from 60-99% often die suddenly without autopsy evidence of acute antemortem thrombosis, or some other acute exacerbation of their disease. Also 1/5 of the saphenous vein bypass grafts presently surgically implanted are not patent when restudied. We postulate that platelets aggregate in narrowed coronary arteries, or tight anastomoses in saphenous vein grafts, and that these platelet plugs may lead to sufficient added coronary obstruction to produce angina, arrhythmias and sudden death. We propose to use an animal model, in which the dogs are given a 60-90% stenosis of the coronary artery and studied with electromagnetic flowmeters. We have evidence to show that platelets do aggregate in the narrowed lumen, that this can be aggrevated by high plasma levels of catecholamines, lipids, or the male hormone testosterone, and that this life threatening platelet plug can be inhibited with moderate doses of aspirin. We plan to study these agents in our animal model, investigating those agents which exacerbate or ameliorate this platelet plugging of the stenosed coronary artery.